We had previously observed that transformation by ras-H of NIH-3T3 cells resulted in metastatic as well as tumorigenic cells. Since cells transformed by v-sarc or v-mos were not metastatic, but were highly tumorigenic, the property of inducing metastasis appeared to be unique to the ras-H gene. We extended this work to ras-H transformed rat embryo cells. These cells were also highly metastatic when transformed either by ras-H or by ras-H linked to an enhancer. However, when the cooperating oncogene Ela was used in conjunction with ras-H, metastasis was only rarely seen. We examined the karyotypes of these cells. Surprisingly, the ras-H transformed rat embryo cells had either remained diploid or near diploid. Even in the metastases in nude mice derived from these cells, the karyotype was unchanged from the parental cell line. This suggests that karyotypic selection does not play a role in the metastatic process for these cells. However, ras-H did not induce metastatic potential in all cell lines tested. For example, C127 cells, a murine epithelioid line, did not metastasize after transformation by ras-H although the cells were highly tumorigenic. Metastatic potential has been induced in these cells by gene transfer and attempts are under way to clone the gene involved.